© 2004 American Thoracic Society
Nicotine and Hypersensitivity PneumonitisTo the Editor:I read with disbelief the conclusions of the recent article by Blanchet and colleagues (1) suggesting that nicotine could be of interest in the treatment of hypersensitivity pneumonitis and other pulmonary inflammatory diseases. To add insult to injury, it was extremely disheartening as a respiratory physician who deals with the catastrophic effects of smoking on a daily basis to have read the article in a leading high impact-factor respiratory journal. The irresponsible conclusions of the authors cannot be left unrebuked. Indeed, the editorial by Maier (2) in the same issue of the Journal discusses the many major health hazards associated with tobacco use and the recognition that although tobacco smoke has immunosuppressive properties, this may in itself contribute to the development of smoking-related diseases through effects on innate and adaptive immunity. If asbestos was found to have similar antiinflammatory properties to nicotine, would anyone recommend this carcinogen as a potential therapeutic agent? We must not lose sight of our responsibility in the dissemination of information and education with regard to the harmful effects of tobacco smoking, instead of investing precious time and effort in the promotion of nicotine use.
Ipswich Hospital Suffolk, United Kingdom FOOTNOTES Conflict of Interest Statement: D.K.C.L. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter. REFERENCES
From the Authors: We appreciate Dr. Lee's concerns of our work on the potential beneficial effects of nicotine in hypersensitivity pneumonitis (1). We never intended to even suggest that cigarette smoking could be recommended in the treatment for this or any other disease. Our conclusion is that targeting one property of nicotine and its mode of action could be of interest in the treatment of hypersensitivity pneumonitis. One has to keep in mind that nicotine is one of more than 4,000 products found in cigarette smoke and it may not be responsible for the major health risks associated with cigarette smoking (2). Nicotine presents protective effects in neurodegenerative disorders; it is also a potent pain killer. Nicotine's biggest drawback is that it crosses the blood–brain barrier and causes addiction. It is therefore by far not an ideal compound. Nicotine is only one of the many molecules that bind to and activate a large subgroup of cholinergic receptors whose natural endogenous ligand is acetylcholine. These nicotinic acetylcholine receptors (nAChrs) have a number of structural diversities and are widely expressed in the nervous system and on many other cells throughout the body including pulmonary inflammatory cells. Stimulation of specific subunits of these receptors produces antiinflammatory effects (3). There are a large number of other natural and synthetic molecules that, like nicotine, act as ligands of the nicotinic receptor. Some of these molecules do not cross the blood–brain barrier, and therefore could be more appropriate therapeutic agents. In our article, we have demonstrated the beneficial effect of nicotine in inflammatory conditions. We used nicotine for its effect on nAChrs and our results show that the protective role of cigarette smoking on certain diseases might be mediated, at least in part, via these receptors. This is pertinent information on the understanding of human diseases and potential targets for future treatments and, as such, we believe that our work was appropriately published in AJRCCM.
Institut Universitaire de Cardiologie et de Pneumologie de l'Université Laval Ste-Foy, Quebec, Canada FOOTNOTES Conflict of Interest Statement: M.-R.B. and E.I.-A. are coinventors of patent #PCT/CAO2/00412, owned by Laval University. Y.C. is the principal inventor of patent #PCT/CAO2/00412, owned by Laval University. REFERENCES
From the Editorialist: In his Letter to the Editor, Dr. Lee rebukes the conclusions by Blanchet and colleagues (1) to consider nicotine as a treatment for hypersensitivity pneumonitis and questions the Journal's publication of this article, which he interprets as promoting nicotine use. While I agree with Dr. Lee (2) that we cannot, and should not, conclude that nicotine or tobacco be used as treatment for this disease based on this article, as pulmonary physicians we would be remiss if we failed to publish and recognize the important implications of the study by Blanchet and colleagues (1). Granulomatous lung diseases, such as hypersensitivity pneumonitis and sarcoidosis, continue to result in significant morbidity and mortality to the individuals affected. Unfortunately, the current treatment for these disease processes relies on nonspecific immunosuppressive therapy, such as prednisone, methotrexate, and azathioprine, together with removal from exposure in the case of hypersensitivity pneumonitis (3, 4). These therapies are fraught with numerous side effects and frequently a lack of response. However, if we can learn how nicotine may inhibit granulomatous inflammation, as suggested in the model by Blanchet and colleagues (1), this important information may help us find other more specific agents or therapies to reduce the immune response and subsequent disease progression in granulomatous diseases, hopefully with fewer side effects and increased efficacy than our current therapies. This would be an important service for us to provide to our patients with these diseases. The model and findings of Blanchet and colleagues (1) provide a steppingstone to achieving this goal. If instead we do not acknowledge these findings because of the author's conclusions and a potential misunderstanding that they are promoting tobacco use, we are providing a disservice to our patients with granulomatous lung disease, much as we would if we failed to acknowledge the significant health hazards of tobacco.
National Jewish Medical and Research Center Denver, Colorado FOOTNOTES Conflict of Interest Statement: L.A.M. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter. REFERENCES
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